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Objective To evaluate the value of detecting HCMV-DNA in urine in the diseases of newborn babies ,by comparing the result between HCMV-DNA in urine and HCMV-IgM antibody in blood in different diseases of the newborn babies .Methods The urine and blood samples were collected from 1 520 infants who were in hospital of the neonate department from January 2013 to December 2014 .The HCMV-DNA in urine was examined by fluorescence quantitative polymerase chain reaction(FQ-PCR) .And HCMV-IgM antibody in blood was examined by the method of chemiluminescence(ECL) .Results In the 1 520 cases ,153 had de-tectable HCMV-DNA in their urine samples with a positive rate 10 .07% ,while only 4 cases were positive of the HCMV-IgM anti-body in blood with a positive rate 0 .27% .The two groups was statistically significant difference (P<0 .05) .In the infant diseases of 1 520 cases ,the positive rate of HCMV-DNA in urine was 82 .6% of the hepatitis syndrome while the positive rate of HCMV-IgM antibody in blood was 3 .85% .The positive rate of HCMV-DNA in urine was 8 .95% in the jaundice symptoms ,while the posi-tive rate HCMV-DNA in urine was 4 .62% in the pulmonary infection .Each group of disease was statistically significant difference in the positive rate of HCMV-DNA (P<0 .05) .Conclusion The detection of HCMV-DNA in urine is more beneficial to the diag-nosis of HCM V infection of infants than the detection of HCM V-IgM antibody in blood ,especially in hepatitis syndrome ,neonatal jaundice and pulmonary infection .
ABSTRACT
Conditional forebrain-specific presenilin-1 and presenilin-2 double knockout mice (dKO mice) exhibit several neurodegenerative phenotypes of Alzheimer's disease (AD) pathology, such as tau hyperphosphorylation, neuron loss, forebrain cortical shrinkage and memory impairment. By using capillary electrophoresis assay, monoamine neurotransmitters in forebrain cortex, hippocampus and other forebrain region of dKO mice aged at 6, 9 and 12 months were measured to illustrate the relationship among presenilins function deficiency, neurodegenerative phenotypes and monoamine neurotransmitters. Data showed that levels of monoamine neurotransmitters in forebrain cortex of dKO mice were significantly decreased at 6 months when compared to controls, while as mice getting older, levels of monoamine neurotransmitters increased to that of controls, or even higher. In hippocampus, 5-hydroxytryptamin and epinephrine in dKO mice had a significant increase at 6 months, followed with a significant increase of each monoamine neurotransmitter at 12 months age. In other forebrain region, 5-hydroxytryptamin and dopamine had a similar level between control and dKO mice at 6 and 9 months but a significant decrease at 12 months; however, level of norepinephrine and epinephrine were significantly decreased at 6 and 12 months except epinephrine of 6 months. These results demonstrated that knockout of presenilins genes could lead to the variation of monoamine neurotransmitters, and the variation profiles were different among forebrain cortex, hippocampus and other forebrain region. However, whether presenilins deficiency caused the variation of monoamine neurotransmitter directly or not, and how about the effects of variation of monoamine neurotransmitters on AD-like pathology need to be further analyzed.
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Objective To explore the mechanism of IL-6 in EAE. Methods 25 female Wistar rats were randomly divided into 2 groups, EAE group( n=15 ) and normal control group( n=10). The expression of IL-6, TNF-αtand TGF-β of the two groups rots were ob-served by immunohistochemistry staining, and then correlation analysis of the expression of IL-6, TNF-αtandTGF-β was made. Results There was negative correlation between gray scale of IL-6 and symptom scores( r=-0.953, P＞0.05). IL-6 and TGF-β had no statistical-ly significant correlation ( r=-0.492, P＞0.05). There was negative correlation between gray scale of TNF-α and symptom scores( r=-0.978, P＜0.05), and both of the correlation between TNF-α and TGF-β ( r=-0.502, P＞0.05), TGF-β and scores( r=0.470,P＞0.05 ) were not statistically significant. Conclusions IL-6 may participate in EAE as a inflammatory factor.
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BACKGROUND: The animals commonly used to induce experimental allergic encephalomyelitis (EAE) in oversea laboratory are rodentia animals such as Lewis rats. But in China we are short of Lewis rats. The un-susceptive animal Wistar rats are inexpensive and plentiful. The adding of pertussis toxin may induce EAE successfully in EAE un-susceptive Wistar rats.OBJECTIVE: To investigate the influence of pertussis toxin injected atdifferent sites in inducing EAE model in un-susceptive Wistar rats.DESIGN: A randomized control animal experiment.SETTING: Institute of Brain Science, Shanxi Datong University.MATERIALS: The study was performed in the Institute of Brain Science of Shanxi Datong University from March to October in 2003. Fifty-eight und adjuvant (CFA) group (n=10).METHODS: Besides routine immunization, each rat in the foot dorsum EAE group and intraperitoneal EAE group was administrated with 005 mL pertussis toxin (containing 5.0×1010 thalli), which were given intraperitoneally and subcutaneously on one hind foot respectively, and the antigen in the CFA group was replaced by CFA.cidence rate and tine of atta ck: In the foot dorsum EAE group, the incidence of EAE was 87.5% (21/24), and the time of attack was at (10.25 ±1.67) days after immunization, which were significantly different from those in the intraperitoneal EAE group [35.7% (9/24), (14.8±l.79) days, P sum EAE group, the change of body mass was (-16.00±7.30) g and the symptomscpre was 3.4±0.7, and those in the intraperitoneal EAE group Therewere no or little infiltration of inflammatory cells in the encephalon and spinal cord of CFA rats. In the EAE rats, there were inflammatory cells infiltrated in the boundary of white matter and gray matter of lumbar intumescence, spinal pia mater, spinal parenehyma, and the boundary of cerebral cortex and medulla, even deep medulla, meninges and around lateral ventricle. There were also mild inflammations in the cerebellum,brainstem and optic chiasma, which were concordant with the observed asynchronism, tic, etc. Hematoxylin and eosin (HE) staining displayed that the infiltrated mononuclear cells assembled in perivascular spaces, which were identified by morphological criteria as lymphocyte and macrophages.Forming typical muff-like changes, the inflammation was less severe in intraperitoneal EAE group than in subcutaneous foot dorsum EAE group.CONCLUSION: The EAE model induced in Wistar rats by Pertussis toxin administered subcutaneously on foot dorsum has the representative course of diseases, pathology change and clinical manifestation and the incidence of diseases is high and the cost is low. So it is a more ideal EAE model inducing method.
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AIM: To explore the mechanism of immune tolerance to experimental autoimmune myasthenia gravis (EAMG) in nasally tolerized rats and Wistar rats. METHOD: [ 3H] thymidine incorporation and solid-phase ELISPOT assay were used. RESULTS: The stimulative index of lymphocyte proliferation responses to acetylcholine receptor (AChR) in popliteal and inguinal lymph nodes (PILN) of EAMG rats was higher than that of nasally tolerized rats on week 3, 5 and 7 post immunization (PI) with AChR plus complete Freund′s adjuvant (CFA), and was higher than that of Wistar rats on week 7 PI ( P